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Anatomical pathology > OBSTRUCTIVE/RESTRICTIVE DISEASE > Flashcards

OBSTRUCTIVE/RESTRICTIVE DISEASE Flashcards

1
Q

Obstructive and Restrictive Lung Diseases

A
  • Chronic non-infectious diffuse pulmonary diseases
  • Diagnosis is based primarily on pulmonary function tests
  • Patients commonly have overlapping features

Obstructive lung diseases
• Characterized by increase in resistance to airflow
• FEV1/FVC ratio of less than 0.7 – Reduced FEV1
• Due to partial or complete obstruction of the airway
• From the trachea to the terminal and respiratory bronchioles

Restrictive diseases
• Characterised by reduced expansion of lung parenchyma and decreased total lung capacity (TLC)
• FEV1/FVC ratio remains normal – Both FEV1 and FVC reduced

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2
Q

CHRONIC OBSTRUCTIVE PULMONARY DISEASE

A
  • Risk factors
  • Discuss common chronic obstructive lung disease, asthma and bronchiectasis
  • Underlying pulmonary pathology of two major Clinicopathologic manifestations
  • Chronic bronchitis and Emphysema.
  • Discuss four major types of emphysema
  • Define and discuss chronic bronchitis
  • Asthma
  • Definition
  • Pathology – pathogenesis, morphological findings
  • Bronchiectasis
  • Pathogenesis and morphological features
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3
Q

obstructive lung disease

A

• Definition (World Health Organisation)
• A common, preventable and treatable disease that is characterized by persistent
respiratory symptoms and airflow limitation that is due to airway and/or alveolar
abnormalities caused by exposure to noxious particles or gases.
• Common obstructive lung diseases
• Emphysema, chronic bronchitis, asthma, and bronchiectasis
• Chronic obstructive pulmonary disease (COPD)
• Chronic bronchitis and Emphysema
• RF - Cigarette smoking

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4
Q

Emphysema

A
  • Irreversible enlargement of the airspaces distal to the terminal bronchiole
  • accompanied by destruction of their walls.
  • Classification – Major subtypes
  • Centriacinar
  • Panacinar
  • Paraseptal
  • Irregular
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5
Q

CENTRIACINAR EMPHYSEMA

A

Emphysema
• Centriacinar
• Most common form - >95% of cases
• Pronounced in the upper lobes - apical segments
• Involves proximal parts of the acini (Respiratory bronchioles) and spares distal
parts (Alveoli)
• Both normal and emphysematous air spaces exist in same acinus
• Severe disease involve distal parts (alveoli) and resemble Panacinar emphysema

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6
Q

• Paraseptal EMPHYSEMA

A

• Involves distal part of acinus (Alveoli), proximal portion is normal (Terminal bronchiole)

  • Severe in the upper half of the lungs
  • More striking adjacent to pleura, septa, and margins of lobules
  • Complication
  • Occurs adjacent to areas of fibrosis, scarring, atelectasis
  • Cause of pneumothorax in young adults

• Characterised by enlarged air spaces ranging from 0.5-2.0cm

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7
Q

• Panacinar EMPHYSEMA

A
  • RF - α1-antitrypsin deficiency
  • Acini are uniformly enlarged from respiratory bronchiole to terminal blind alveoli
  • Affects lower zones and anterior margins of lung
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8
Q

Irregular emphysema

A
  • Airspace enlargement with fibrosis (irregular emphysema)
  • Irregularly involvement of acinar parts
  • Associated with scarring
  • Usually clinically insignificant
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9
Q

pathogenesis of emphysema

A

-Toxic injury and inflammation
• Damage to respiratory epithelium  Inflammation → variable degrees of parenchymal destruction

-Protease-antiprotease imbalance
• Relative deficiency of protective antiproteases → Breakdown of connective tissue components by Proteases

-Oxidative stress
• Oxidants → Tissue damage, endothelial dysfunction and inflammation
-
Infection
• exacerbation of existing disease
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10
Q

Gross morphology of emphysema

A
  • Voluminous lungs that overlap heart in the chest cavity
  • Usually, the upper 2/3 are more involved
  • Apical bullae may be present.
  • Cut surface
  • Large alveolar spaces are seen
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11
Q

Microscopy of Emphysema

A
  • Abnormally large alveoli separated by thin septa with focal Centriacinar fibrosis.
  • Dilated pores of Kohn
  • Club shaped septa
  • Small airway inflammation
  • Inflammatory infiltrates in bronchial walls
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12
Q

clinical feautures of emphysema

A

• Barrel-chest
• Dyspnoea
• Impaired expiratory airflow is the key to diagnosis
-Prolonged expiration
-Often referred to as “Pink puffers”
=Patients sits forward in hunched-over position and breathes through pursed lips - Puffer
=Blood-gas values relatively normal at rest as the patient over-ventilate to remain oxygenated - Pink

• Poor prognosis with development of Cor-pulmonale
-Congestive heart failure and secondary pulmonary hypertension

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13
Q

Treatment of emphysema

A
  1. Smoking cessation
  2. Oxygen therapy
  3. Long-acting bronchodilators
  4. Inhaled corticosteroids
  5. Physical therapy
  6. Bullectomy
  7. Lung volume reduction surgery
  8. Lung transplantation
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14
Q

Other conditions associated with lung over inflation

A

• Compensatory hyperinflation
-dilation of alveoli in response to loss of lung substance elsewhere
• Obstructive over inflation
- air trapping leading to hyperinflation – foreign body
• Bullous emphysema
-large sub pleural bullae ≥ 1 cm
• Interstitial emphysema
-entrance of air into the connective tissue stroma of the lung,
mediastinum, or subcutaneous tissues

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15
Q

Chronic Bronchitis

A

• Persistent, productive cough ≥ 3 months ≥ 2 consecutive years in the absence of any other
identifiable cause
• Common in habitual smokers / smog-laden cities

Major risk factor
• Cigarette smoke
• Damages epithelium
• Chronic inflammation
• Interferes with muco-ciliary action of the respiratory epithelium
• Prevents clearance of mucus → increasing the risk of infection

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16
Q

Pathogenesis of chronic bronchitis

A
  1. Mucus hypersecretion
  2. Acquired (CFTR) dysfunction
  3. Inflammation
  4. Infection
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17
Q

Gross morphology of bronchitis

A
  • Hyperemia, swelling and oedema of mucous membranes
  • Associated mucinous or mucopurulent secretions
  • May see casts of mucus and exudate in airways
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18
Q

Chronic Bronchitis

• Microscopy

A
  • Characteristic microscopic features
  • Chronic inflammation of the airways
  • Thickened bronchiolar wall
  • smooth muscle hypertrophy
  • Deposition of extracellular matrix in the muscle layer
  • Peri-bronchial fibrosis

• Goblet cell hyperplasia
• Enlargement of the mucus-secreting glands of the trachea and bronchi.
• Increase in the size of the mucous glands
• Assessed by Reid index - normally = 0.4
» the ratio of the thickness of the mucous gland layer to the thickness of the wall
between the epithelium and the cartilage .
• Narrowing of bronchioles → bronchiolitis obliterans.
• Squamous metaplasia - dysplasia

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19
Q

cardinal symptoms of Chronic Bronchitis

A
  • Persistent cough
  • Productive of sputum
  • Dyspnoea on exertion
  • Hypercapnia, hypoxemia, mild cyanosis

“Blue bloaters”
• Accelerate decline in lung function
• Cor pulmonale and heart failure

20
Q

differences between bronchitis and emphysema

A

Bronchitis

Age:40-45
Dyspnea: Mild; late
Cough: Early, copious sputum
infections: Common
respiratory insufficiency; Early periodic
Cor pulmonale: Common
airway resistance: Increased
Elastic recoil: Normal
chest radiograph: Prominent vessels, large heart size
Appearance: Blue bloater
Emphysema
Age:50-75
Dyspnea: Severe; early
Cough: Late; scanty sputum
Infections; Occasional
respiratory insufficiency: End-stage
Cor pulmonale: Uncommon, End-stage
Airway resistance: Normal or slightly
increased
Elastic recoil: Low
Chest radiograph: Hyperinflation; normal heart size
Appearance: Pink puffer
21
Q

asthma

A

• Heterogenous disorder of the conducting airways usually caused by an immunological process marked by episodic bronchoconstriction, inflammation of the bronchial walls; and increased mucus secretion

• Classification
 -Atopic
• IgE-mediated (type I) hypersensitivity reaction
• Onset - childhood
• Triggered by environmental allergens

-Non-atopic
•No evidence of allergen sensitization

-Drug induced
• Aspirin-sensitive asthma

-Occupational

22
Q

pathogenesis of asthma(Th2 Responses, IgE, and Inflammation)

A

• Presentation of antigen to naïve CD4+ helper T cells

-IL-4
• Stimulates class switching to IgE and promotes the development of additional Th2 cells
  • IL-5
    • Development and activation of eosinophils

-IL-13
• Enhances IgE production
• Stimulate mucus secretion by epithelial cells

23
Q

Pathogenesis of Asthma (Sensitization and activation of Mast Cells)

A
  • Activated by high-affinity IgE Fc receptors
  • Release of mediators by mast cell (degranulation)
  • Vasoactive amines. – histamine
    » Smooth muscle contraction
    » Increases vascular permeability
    » Mucus secretion.
  • Enzymes – Proteases (Chymase/Tryptase)
    » tissue damage
  • Proteoglycans – heparin and chondroitin sulphate
    » package and store the amines
24
Q

Pathogenesis of asthma (Sensitization and activation of Mast Cells)

A

• Lipid mediators
- Leukotrienes
» Leukotrienes C4 and D4 are vasoactive and spasmogenic,
» Leukotriene B4 is highly chemotactic for neutrophils, eosinophils, and monocytes.

  • Prostaglandin D2.
    » Causes intense bronchospasm and mucus hypersecretion secretion.

-Platelet-activating factor (PAF)
» causes platelet aggregation, histamine release, bronchospasm, increased vascular permeability, and vasodilation

25
Q

Status asthmaticus

A
  • Unremitting asthmatic attack
  • Lungs are distended by over inflation
  • Small areas of atelectasis
  • Most striking: occlusion of bronchi and bronchioles by thick mucus plugs
26
Q

Sputum(of asthma)

A
  • Curschmann spirals
  • Extrusion of mucus plugs from mucous glands
  • Numerous eosinophils
  • Charcot-Leyden crystals
  • Composed of eosinophil protein galectin-10
27
Q

Asthma

• Microscopy - Airway remodeling

A
  1. Thickening of airway wall
  2. Sub-basement membrane fibrosis
  3. Increased vascularity
  4. Increase in size of submucosal glands
  5. Increase in number of airway goblet cells
  6. Hypertrophy + hyperplasia of bronchial smooth muscle
28
Q

Asthma

Clinical features

A
  • Chest tightness, dyspnea, wheezing, coughing (+/- sputum)
  • Classic attack - several hours
  • Status asthmaticus – days or even weeks
  • Between the attacks, patients may be virtually asymptomatic
29
Q

Bronchiecstasis

A

• Bronchiectasis is a disorder in which destruction of smooth muscle and elastic tissue by chronic
necrotising infections leads to permanent dilation of bronchi and bronchioles

• Associated with
• Congenital or hereditary conditions that predispose to chronic infections (cystic fibrosis),
immunodeficiency states, primary ciliary dyskinesia, and Kartagener syndrome.
• Severe necrotizing pneumonia
• Bronchial obstruction
• Immune disorders
• idiopathic

30
Q

pathogenesis of bronchiecstasis

A

Obstruction and infection

31
Q

Gross Morphology of bronchiecstasis

A
  • Affects lower lobes bilaterally
  • May be diffuse or localised
  • Dilated airways – up to 4x in size
  • Bronchi can be followed to pleural surface
  • Bronchi appear cystic and are filled with mucopurulent secretions
32
Q

Bronchiectasis

• Microscopy

A

• Acute and chronic inflammatory exudation
• Desquamation of epithelial lining
• Ulceration
• Squamous metaplasia of the remaining epithelium
• Necrosis destroys the bronchial or bronchiolar walls and forms
a lung abscess
• Fibrosis of the bronchial and bronchiolar walls

33
Q

Exudation of bronchiecstasis

A

The bronchus has residual epithelium (Square) with necrotizing inflammation (Circle) with subsequent bronchial
destruction, and inflammation extending into the adjacent lung parenchyma, characteristic of bronchiectasis

34
Q

symptoms/signs of bronchiectasis

A
  • Sever persistent cough
  • Foul smelling, sometimes bloody, sputum
  • Dyspnoea and orthopnea in severe cases
  • Hemoptysis – may be massive
  • Exacerbated by URTI
35
Q

Restrictive lung diseases

A

• characterized by inflammation and fibrosis of the lung interstitium
associated with pulmonary function studies indicative of restrictive
lung disease.
• Reduction in diffusion capacity, lung volume, and lung compliance
• Chronic Diffuse Interstitial (Restrictive) Diseases
• Chest wall disorders
• Neuromuscular diseases such as poliomyelitis
• Severe obesity
• Pleural diseases
• Kyphoscoliosis

36
Q

• Chronic Diffuse Interstitial (Restrictive) Diseases

A
  • Chronic interstitial and infiltrative diseases
  • Interstitial fibrosis of unknown etiology
  • Idiopathic Pulmonary Fibrosis
  • Nonspecific Interstitial Pneumonia
  • Cryptogenic Organizing Pneumonia
  • Pulmonary Involvement in Autoimmune Diseases
  • Pneumoconiosis
37
Q

Idiopathic Pulmonary fibrosis (cryptogenic fibrosing alveolitis)

A

• progressive interstitial pulmonary fibrosis and respiratory failure

  • Pattern of lung injury – usual interstitial pneumonitis
  • Patchy  subpleural regions and lower lobes
  • Fibrosis in various stages of development
  • Variable inflammation
38
Q

• Morphology of Idiopathic Pulmonary fibrosis (cryptogenic fibrosing alveolitis)

A
  • Usual interstitial pneumonia (UIP)
  • Gross – Cobblestone pleural surface
  • Retraction of scars along the interlobular septa
  • Firm, rubbery white areas of fibrosis
  • Affects lower lobes, the sub pleural regions, and along the interlobular septa
39
Q

microscopy of Idiopathic Pulmonery fibrosis (cryptogenic fibrosing alveolitis)

A

• Hallmark - patchy interstitial fibrosis of varying age and intensity
» Early lesion – Hypercellular - fibroblastic foci
» Late lesion – Hypocellular, dense fibrosis with destruction of alveolar architecture
» Honeycomb fibrosis - formation of cystic spaces lined by hyperplastic type II pneumocytes or
bronchiolar epithelium
» Mild to moderate inflammation
» Squamous metaplasia and smooth muscle hyperplasia
» Pulmonary hypertension - intimal fibrosis and medial thickening
» acute exacerbations - DAD

40
Q

Restrictive lung diseases

Clinical features

A
  • Progressive dyspnoea
  • Dry cough
  • Clubbing
  • Fatigue and weight loss
  • Progress to respiratory failure in 5years
41
Q

Factors that influence the development of dust-borne pneumoconiosis

A

• Dust retention - dust concentration, duration of exposure, and effectiveness of clearance mechanisms
• Particle size - dangerous particles are from 1 to 5 μm in diameter because they can reach the terminal
small airways and air sacs
• Particle solubility and cytotoxicity
• Particle uptake by epithelial cells or egress across epithelial linings
• Activation of the inflammasome which occurs following phagocytosis
• Tobacco smoking, which worsens the effects of all inhaled mineral dusts, but particularly those caused
by asbestos.

42
Q

Pneumoconiosis

A

• non-neoplastic lung reaction to inhalation of mineral dusts encountered in the workplace, now also includes disease induced
by chemical fumes and vapors

43
Q

Coal Workers’ Pneumoconiosis

A
  • Inhalation of coal particles
  • Anthracosis
  • Coal macules - 1 to 2 mm in diameter
  • if larger = Nodules.
  • Carbon-laden macrophages;
  • Delicate network of collagen fibers.
  • Located primarily adjacent to respiratory bronchioles
44
Q

silicosis

A

Silicosis
• Inhalation of pro-inflammatory crystalline silicon dioxide (silica)
• Early stages - Small, barely palpable, discrete pale to blackened nodules in hilar
lymph nodes and upper zones of the lungs.

  • Late stages - Hard, collagenous scars
  • Softening and cavitation - superimposed tuberculosis or to ischemia.
  • Hallmark lesion
  • Central area of whorled collagen fibers with a more peripheral zone of dust-laden macrophages
  • Examination of the nodules by polarized microscopy reveals weakly birefringent silicate particles
45
Q

Asbestosis

A

Asbestosis
• Inhalation of pro-inflammatory crystalline hydrated silicates that are associated with pulmonary
fibrosis and various forms of cancer – activation of inflammasome

Asbestosis
• Diffuse pulmonary interstitial fibrosis

• Presence of asbestos bodies
• Golden brown, fusiform or beaded rods with a translucent center that consist of asbestos fibers coated
with an iron-containing proteinaceous material
• They arise when macrophages phagocytose asbestos fibers; the iron is derived from phagocyte ferritin
• Similar iron-protein complexes called ferruginous bodies.

  • Early
  • Fibrosis around respiratory bronchioles
  • Late stages
  • Pleural plaques - Well-circumscribed plaques of dense collagen + calcified
46
Q

Asbestos-related disease:

A
  • Recurrent pleural effusion
  • Parenchymal interstitial fibrosis - asbestosis
  • Lung carcinoma
  • Mesothelioma
  • Laryngeal, ovarian neoplasms
  • Increased risks for systemic autoimmune diseases and cardiovascular disease

Anatomical pathology (13 decks)

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